The human heart has four valves which control the direction of blood flow in the circulation. The aortic and mitral valves are part of the “left” heart and control the flow of oxygen-rich blood from the lungs to the body, while the pulmonic and tricuspid valves are part of the “right” heart and control the flow of oxygen-depleted blood from the body to the lungs. The aortic and pulmonic valves lie between a pumping chamber (ventricle) and major artery, preventing blood from leaking back into the ventricle after it has been ejected into the circulation. The mitral and tricuspid valves lie between a receiving chamber (atrium) and a ventricle preventing blood from leaking back into the atrium during ejection.
Various disease processes can impair the proper functioning of one or more of these valves. These include degenerative processes (e.g., Barlow's Disease, fibroelastic deficiency), inflammatory processes (e.g., Rheumatic Heart Disease) and infectious processes (e.g., endocarditis). In addition, damage to the ventricle from prior heart attacks (i.e., myocardial infarction secondary to coronary artery disease) or other heart diseases (e.g., cardiomyopathy) can distort the valve's geometry causing it to dysfunction.
Heart valves can malfunction in one of two ways. Valve stenosis is present when the valve does not open completely causing a relative obstruction to blood flow. Valve regurgitation is present when the valve does not close completely causing blood to leak back into the prior chamber. Both of these conditions increase the workload on the heart and are very serious conditions. If left untreated, they can lead to debilitating symptoms including congestive heart failure, permanent heart damage and ultimately death. Dysfunction of the left-sided valves—the aortic and mitral valves—is typically more serious since the left ventricle is the primary pumping chamber of the heart.
Dysfunctional valves can either be repaired, with preservation of the patient's own valve, or replaced with some type of mechanical or biologic valve substitute. Since all valve prostheses have some disadvantages (e.g., need for lifelong treatment with blood thinners, risk of clot formation and limited durability), valve repair, when possible, is usually preferable to replacement of the valve. Many dysfunctional valves, however, are diseased beyond the point of repair. In addition, valve repair is usually more technically demanding and only a minority of heart surgeons are capable of performing complex valve repairs. The appropriate treatment depends on the specific valve involved, the specific disease/dysfunction and the experience of the surgeon.
The aortic valve is more prone to stenosis, which typically results from buildup of calcified material on the valve leaflets and usually requires aortic valve replacement. Regurgitant aortic valves can sometimes be repaired but usually also need to be replaced. The pulmonic valve has a structure and function similar to that of the aortic valve. Dysfunction of the pulmonic valve, however, is much less common and is nearly always associated with complex congenital heart defects. Pulmonic valve replacement is occasionally performed in adults with longstanding congenital heart disease.
Mitral valve regurgitation is more common than mitral stenosis. Although mitral stenosis, which usually results from inflammation and fusion of the valve leaflets, can often be repaired by peeling the leaflets apart (i.e., a commisurotomy), as with aortic stenosis, the valve is often heavily damaged and may require replacement. Mitral regurgitation, however, can nearly always be repaired but successful repair requires a thorough understanding of the anatomy and physiology of the valve, of the types of mitral valve dysfunction leading to mitral regurgitation and the specific diseases and lesions resulting in this dysfunction.
The normal mitral valve can be divided into three parts—an annulus, a pair of leaflets and a sub-valvular apparatus. The annulus is a dense ring of fibrous tissue which lies at the juncture between the left atrium and left ventricle. The annulus is normally elliptical or more precisely “kidney-shaped” with a vertical (anteroposterior) diameter approximately two-thirds of the horizontal diameter. The larger elliptical anterior leaflet and the smaller, crescent-shaped posterior leaflet attach to the annulus. Approximately two-thirds of the annulus is attached to the posterior leaflet and one-third to the anterior leaflet. The edge of the leaflet which is not attached to the annulus is known as the free margin. When the valve is closed, the free margins of the two leaflets come together within the valve orifice forming an arc in the shape of a “smile” known as the line of coaptation. The corners of this “smile”, the two points on the annulus where the anterior and posterior leaflets meet (at approximately the 10 o'clock and 2 o'clock positions), are known as the commisures. The posterior leaflet is usually separated into three distinct scallops by small clefts which are referred to (from left to right) as P1, P2 and P3. The corresponding portions of the anterior leaflet directly opposite P1, P2 and P3 are referred to as A1, A2 and A3. The sub-valvular apparatus consists of two thumb-like muscular projections from the inner wall of the left ventricle known as papillary muscles and numerous chordae tendinae (or simply “chords”) which are thin fibrous bundles which emanate from the tips of the papillary muscles and attach to the free margin or undersurface of the valve leaflets in a parachute-like configuration.
The normal mitral valve opens when the left ventricle relaxes (diastole) allowing blood from the left atrium to fill the decompressed left ventricle. When the left ventricle contracts (systole), the increase in pressure within the ventricle causes the valve to close, preventing blood from leaking into the left atrium and assuring that all of the blood leaving the left ventricle (the stroke volume) is ejected through the aortic valve into the aorta and to the body. Proper function of the valve is dependent on a complex interplay between the annulus, leaflets and subvalvular apparatus.
Lesions in any of these components can cause the valve to dysfunction, leading to mitral regurgitation. Physiologically, mitral regurgitation results in increased cardiac work since the energy consumed to pump some of the stroke volume of blood back into the left atrium is wasted. It also leads to increased pressures in the left atrium which results in back up of fluid in the lungs and shortness of breath—a condition known as congestive heart failure.
Mitral valve dysfunction leading to mitral regurgitation can be classified into three types based of the motion of the leaflets (known as “Carpentier's Functional Classification”). Type I dysfunction occurs despite normal leaflet motion. Lesions which can cause Type I dysfunction include a hole in the leaflet (usually from infection) or much more commonly distortion and dilatation of the annulus. Annular dilatation or distortion results in separation of the free margins of the two leaflets. This gap prevents the leaflets from coapting allowing blood to regurgitate back into the left atrium during systolic contraction.
Type II dysfunction results from leaflet prolapse. This occurs when a portion of the free margin of one or both leaflets is not properly supported by the subvalvular apparatus. During systolic contraction, the free margins of the involved portions of the leaflets prolapse above the plane of the annulus into the left atrium. This prevents leaflet coaptation and allows blood to regurgitate into the left atrium between the leaflets. The most common lesions resulting in leaflet prolapse and Type II dysfunction include chordal elongation or rupture due to degenerative changes (such as myxomatous pathology or “Barlow's Disease” and fibroelastic deficiency) or prior myocardial infarction.
Finally, Type III dysfunction results from restricted leaflet motion. Here, the free margins of portions of one or both leaflets are pulled below the plane of the annulus into the left ventricle. This prevents the leaflets from rising up to the plane of the annulus and coapting during systolic contraction. The restricted leaflet motion can be related to valvular or subvalvular pathology (usually fibrosis following damage from rheumatic heart disease)—referred to as Type IIIA dysfunction. It more commonly occurs when abnormal ventricular geometry or function leads to papillary muscle displacement which pulls the otherwise normal leaflets down into the ventricle, away from each preventing proper coaptation of the leaflets. This is known as Type IIIB dysfunction and usually results from prior myocardial infarction (“ischemia”) or severe ventricular dilatation and dysfunction (“cardiomyopathy”).
The anatomy and function of the tricuspid valve is similar to that of the mitral valve. It also has an annulus, chords and papillary muscles but has three leaflets (anterior, posterior and septal). The shape of the annulus is slightly different, more snail-shaped and slightly asymmetric. The demands on the tricuspid valve are significantly less than the mitral valve since the pressures in the right heart are normally only about 20% of the pressures in the left heart. Tricuspid stenosis is very rare in adults and usually results from very advanced rheumatic heart disease. Tricuspid regurgitation is much more common and can result from the same types of dysfunction (I, II, IIIA and IIIB) as the mitral valve. The vast majority of patients, however, have Type I dysfunction with annular dilatation preventing leaflet coaptation. This is usually secondary to left heart disease (valvular or ventricular) which can, over time, lead to increased pressures back stream in the pulmonary arteries, right ventricle and right atrium. The increased pressures in the right heart can lead to dilatation of the chambers and concomitant tricuspid annular dilatation.
The benefits of valve repair over replacement are now well established in the cardiac surgical literature in all types of valve dysfunction and in nearly all disease states. Patients undergoing valve repair have been shown to live longer, with better preservation of cardiac function. The vast majority of patients with mitral or tricuspid regurgitation can have their valves successfully repaired instead of replaced. The likelihood of a successful repair, however, is highly dependent on the skill, knowledge and experience of the individual surgeon. Although most surgeons are comfortable performing simple valve repairs (annuloplasty rings, limited leaflet resections, etc.), many rarely perform valve repairs and only a small minority of surgeons is facile at more complex valve repairs. Most surgeons have inadequate knowledge and training in these techniques and, even if they had the technical ability, they do not encounter enough patients to feel comfortable with complex cases. This variability in surgical skill is reflected in the wide range of valve repair rates among different centers. High-volume, experienced centers routinely report valve repair rates over 90% while the national average is only 20-30%.
A typical mitral valve repair involves various procedures or stages, each one correcting a specific abnormality of a specific component of the valve apparatus. Specific techniques are available for each component (annulus, leaflet segments, chords, and papillary muscles) of the valve. The annular circumference and shape can be restored with an annuloplasty device (ring or band) which is attached to the annulus using sutures. Annular calcification can be excised. Excess or prolapsing leaflet tissue can be resected and reconstructed. Shrunken or restricted leaflet segments can be augmented with a patch of autologous tissue. Leaflet segments can be partially detached from the annulus and advanced to cover a gap from a leaflet resection (known as a sliding valvuloplasty). Ruptured or elongated chords can be replaced with artificial chords or by transferring redundant chords from another leaflet segment. Shrunken or fused chords can be released or split. Occasionally, the papillary muscles themselves can be shortened to correct prolapse from multiple elongated chords.
The power of Carpentier's functional classification system is that the appropriate surgical techniques derive directly from the type of dysfunction. Patients with Type I valve dysfunction (normal leaflet motion due to annular dilatation) and Type IIIB valve dysfunction (restricted leaflet motion due to ventricular distortion) can usually be repaired with implantation of an annuloplasty ring alone. In Type I valve dysfunction, the annuloplasty is sized based on the dimensions of the anterior leaflet to restore the annulus to its original size. In Type IIIB valve dysfunction, the annuloplasty must be downsized to account for restricted leaflet motion.
Patients with Type II and IIIA valve dysfunction usually require more complex repairs. Type IIIA valve dysfunction (restricted leaflet motion due to valvular/subvalvular pathology) can require leaflet augmentation and/or chordal release/splitting. Type II valve dysfunction (leaflet prolapse) usually requires some type of leaflet resection and reconstruction along with, on occasion, additional leaflet and chordal procedures. The most common type of valve repair for Type II valve dysfunction is a quadrangular resection of the middle (P2) segment of the posterior leaflet with advancement and approximation of the remaining (P1 and P3) segments (a sliding valvuloplasty). Many surgeons are comfortable repairing straightforward cases of P2 prolapse. More complex Type II cases, including those with anterior leaflet involvement or prolapse at or near the commisures, usually require additional procedures such as chordal transfer, placement of artificial chords or additional leaflet resections. Most surgeons, outside of specialized centers, rarely tackle these complex repairs and these patients usually receive a valve replacement. New devices or techniques which simplify complex Type II repairs would greatly expand the proportion of patients who benefit from valve repair over replacement.
Nearly all experienced valve repair surgeons agree that all patients undergoing mitral valve repair must have an annuloplasty procedure performed to assure a successful, durable repair. The annuloplasty serves two main purposes. It restores the shape and size of the annulus to permit adequate leaflet coaptation and prevent regurgitation. It also serves to stabilize any additional repair work by taking tension off of any suture lines. Although annuloplasties were originally performed using a suture woven in and out of the annulus like a purse string, nearly all surgeons today utilize a prosthetic annuloplasty device. This is usually a prosthetic ring or band that is attached within the heart to the dilated and distorted annulus using multiple sutures. The annuloplasty usually includes an inner frame made of metal, such as stainless steel or titanium, or of a flexible material, such as silicone rubber or Dacron cordage, and is covered with a biocompatible fabric or cloth into which the sutures are placed. The rings may be rigid, semi-rigid or flexible, and they may form a complete continuous ring, a split ring or a partial ring or band. Annuloplasty rings may be provided in one of several shapes—circular, D- or “kidney” shaped or C-shaped. Rings are usually specifically designed for the mitral or tricuspid valves. An annuloplasty ring system usually consists of rings of various sizes (24 to 40 mm) loaded on specialized holders to facilitate placement along with a series of sizers to measure the dimensions of the patient's valve.
Common examples of rigid annuloplasty rings are the original Carpentier ring disclosed in U.S. Pat. No. 3,656,185, the more current Carpentier-Edwards® ring (distributed by Edwards Laboratories) disclosed in U.S. Pat. No. 5,061,277, and the ring disclosed in U.S. Pat. No. 4,164,046, which are hereby incorporated by reference. Examples of semi-rigid annuloplasty rings include the Carpentier-Edwards Physio™ ring as disclosed in U.S. Pat. No. 5,104,407 and the ring disclosed in U.S. Pat. No. 4,489,446, which are hereby incorporated by reference. Common examples of flexible rings include the Duran ring (distributed by Medtronic) as disclosed in Duran et al., Circulation (Suppl. I) 78:91-96(1989) and the Puig-Massana ring as disclosed in U.S. Pat. No. 4,290,151, which are hereby incorporated by reference. Other annuloplasty rings include the Seguin Ring (made by St. Jude), the Carbomedics rings, the Colvin-Galloway Ring (made by Medtronic), the Carpentier Tricuspid Ring and the Edwards MC3 Tricuspid Ring.
Each of these types of annuloplasty rings has advantages and disadvantages that are commonly understood in the field of mitral valve repair. Rigid and semi-rigid rings are believed to more completely restore the shape as well as the circumference of the annulus. As such they are said to perform a “remodeling” (shape restoring) annuloplasty in addition to a “reduction” (circumference decreasing) annuloplasty. It has been shown experimentally that restoring and fixing the vertical (anteroposterior) dimension of the annulus is critical to restoring leaflet coaptation and thus to a successful annuloplasty procedure. Rigid and semi-rigid rings more reliably fix this dimension than flexible rings. Flexible rings, however, are somewhat easier to insert and secure to the annulus which might decrease the (albeit low) incidence of post-operative ring detachment (“dehiscence”). They are also purported to preserve the normal three dimensional “saddle” shape of the annulus and its complex motion during the cardiac cycle. Complete rings (rigid or flexible) have the advantage of fixating the entire annulus which should decrease the incidence of late failures due to progressive dilatation of the annulus. Partial rings (more precisely bands) are designed to reduce and fixate the posterior annulus only and are based on the fact that the anterior third of the annulus is part of the fibrous skeleton of the heart and should be less prone to dilate. The advantage of a partial band is that it requires less sutures to secure and eliminates the anterior annular sutures which are typically the most difficult to visualize and place.
Since they involve work inside the heart chambers, conventional procedures for replacing or repairing cardiac valves require the use of the heart-lung machine (cardiopulmonary bypass) and stopping the heart by clamping the ascending aorta and perfusing it with high-potassium solution (cardioplegic arrest). Although most patients tolerate limited periods of cardiopulmonary bypass and cardiac arrest well, these maneuvers are known to adversely affect all organ systems. The most common complications of cardiopulmonary bypass and cardiac arrest are stroke, myocardial “stunning” or damage, respiratory failure, kidney failure, bleeding and generalized inflammation. If severe, these complications can lead to permanent disability or death. The risk of these complications is directly related to the amount of time the patient is on the heart-lung machine (“pump time”) and the amount of time the heart is stopped (“crossclamp time”). Although the safe windows for pump time and cross clamp time depend on individual patient characteristics (age, cardiac reserve, comorbid conditions, etc.), pump times over 4 hours and clamp times over 3 hours can be concerning even in young, relatively healthy patients. Complex valve repairs can push these time limits even in the most experienced hands. Even if he or she is fairly well versed in the principles of mitral valve repair, a less experienced surgeon is often reluctant to spend 3 hours trying to repair a valve since, if the repair is unsuccessful, he or she will have to spend up to an additional hour replacing the valve. Thus, time is a major factor in deterring surgeons from offering the benefits of valve repair over replacement to more patients. Devices and techniques which simplify and expedite valve repair would go a long way to eliminating this deterrent.
Within recent years, there has been a movement to perform many cardiac surgical procedures “minimally invasively” using smaller incisions and innovative cardiopulmonary bypass protocols. The purported benefits of these approaches include less pain, less trauma and more rapid recovery. This has included “off-pump coronary artery bypass” (OPCAB) surgery which is performed on a beating heart with the use of cardiopulmonary bypass and “minimally invasive direct coronary artery bypass” (MIDCAB) which is performed through a small thoracotomy incision. A variety of minimally invasive valve repair procedures have been developed whereby the procedure is performed through a small incision with or without videoscopic assistance and, more recently, robotic assistance. However the use of these minimally invasive procedures has been limited to a handful of surgeons at specialized centers. Even in their hands, the most complex valve repairs cannot be performed since dexterity is limited and the whole procedure moves more slowly. Devices and techniques which simplify valve repair have the potential to greatly increase the use of minimally invasive techniques which would significantly benefit patients.
Thus, it is desirable to provide a single device which, when operatively used, only requires a simplified procedure by which to repair a cardiac valve, and a mitral valve in particular. For example, it would be beneficial to provide a device which, when properly implanted, not only remodels the defective valve annulus but also corrects other problems, such as leaflet prolapse, thereby obviating the need to perform ancillary procedures to correct leaflet size and shape, to reattach or shorten chordae, etc. With such a device, most patients with Type II valve dysfunction could be corrected by device implantation alone or with a limited P2 leaflet resection. Many patients with Type IIIA valve dysfunction could be corrected with aggressive leaflet mobilization (chordal cutting) followed by device implantation. Simplifying the repair procedure would decrease the amount of time the patient's heart would need to be stopped and bypassed with a heart-lung machine and increase the likelihood that it could be performed minimally invasively. This would not only decrease the potential for complications, it would also allow a broader group of surgeons to perform the procedure.